ArticleBMC cancer2017
Tartrate-resistant acid phosphatase (TRAP/ACP5) promotes metastasis-related properties via TGFβ2/TβR and CD44 in MDA-MB-231 breast cancer cells.
Article in BMC cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 42 citations in OpenAlex.
- Integrative transcriptomic analysis identifies ACP5 and FBLN5 as candidate shared transcriptomic signatures between pulpitis and carotid plaque rupture.Scientific reports · 2026Article
- TRAP5 Inhibition Targeting Scar-Associated Macrophages Ameliorates Acute Kidney Injury to Chronic Kidney Disease Transition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- LILRB1 Is a Prognostic-Related Biomarker Correlated With Immune Infiltration in Head-Neck Squamous Cell Carcinoma.Cancer medicine · 2026Article
- Differential contribution of TFE3 isoforms to cell motility and invasion.EMBO reports · 2026Article
- Integrated profiling of metaplastic breast cancer identifies putative master regulators of intratumoral heterogeneity.NPJ breast cancer · 2025Article
- The regulatory role of ACP5 in the diesel exhaust particle-induced AHR inflammatory signaling pathway in a human bronchial epithelial cell line.Scientific reports · 2025Article
- Resolving tumor microenvironment heterogeneity to forecast immunotherapy response in triple-negative breast cancer through multi-scale analysis.Frontiers in oncology · 2025Article
- Inhibition of tartrate-resistant acid phosphatase 5 can prevent cardiac fibrosis after myocardial infarction.Molecular medicine (Cambridge, Mass.) · 2024Article
- Review
- Effects of Low-Phosphorus Diets Supplemented with Phytase on the Production Performance, Phosphorus-Calcium Metabolism, and Bone Metabolism of Aged Hy-Line Brown Laying Hens.Animals : an open access journal from MDPI · 2023Article
- Interleukin-1 alpha and high mobility group box-1 secretion in polyinosinic:polycytidylic-induced colorectal cancer cells occur via RIPK1-dependent mechanism and participate in tumourigenesis.Journal of cell communication and signaling · 2023Article
- Association of ACP5 with the tumor immune microenvironment and its role in cell proliferation and metastasis in pancreatic cancer.American journal of translational research · 2023Article
- NSrp70 suppresses metastasis in triple-negative breast cancer by modulating Numb/TβR1/EMT axis.Oncogene · 2022Article
- Tartrate-resistant acid phosphatase 5 promotes pulmonary fibrosis by modulating β-catenin signaling.Nature communications · 2022Article
- Identification of Iron Metabolism-Related Genes as Prognostic Indicators for Lower-Grade Glioma.Frontiers in oncology · 2021Article
- Tartrate-Resistant Acid Phosphatase 5/ACP5 Interacts with p53 to Control the Expression of SMAD3 in Lung Adenocarcinoma.Molecular therapy oncolytics · 2020Article
- Cathepsin K regulates localization and secretion of Tartrate-Resistant Acid Phosphatase (TRAP) in TRAP-overexpressing MDA-MB-231 breast cancer cells.BMC molecular and cell biology · 2020Article
- Kockdown of ACP5 inhibits hepatocellular carcinoma progression.American journal of translational research · 2020Article
- TopControl: A Tool to Prioritize Candidate Disease-associated Genes based on Topological Network Features.Scientific reports · 2019Article
- Overexpressed ACP5 has prognostic value in colorectal cancer and promotes cell proliferation and tumorigenesis via FAK/PI3K/AKT signaling pathway.American journal of cancer research · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTartrate-resistant acid phosphatase (TRAP/ACP5), a metalloenzyme that is characteristic for its expression in activated osteoclasts and in macrophages, has recently gained considerable focus as a driver of metastasis and was associated with clinically relevant parameters of cancer progression and cancer aggressiveness.
methodsMDA-MB-231 breast cancer cells with different TRAP expression levels (overexpression and knockdown) were generated and characterized for protein expression and activity levels. Functional cell experiments, such as proliferation, migration and invasion assays were performed as well as global phosphoproteomic and proteomic analysis was conducted to connect molecular perturbations to the phenotypic changes.
resultsWe identified an association between metastasis-related properties of TRAP-overexpressing MDA-MB-231 breast cancer cells and a TRAP-dependent regulation of Transforming growth factor (TGFβ) pathway proteins and Cluster of differentiation 44 (CD44). Overexpression of TRAP increased anchorage-independent and anchorage-dependent cell growth and proliferation, induced a more elongated cellular morphology and promoted cell migration and invasion. Migration was increased in the presence of the extracellular matrix (ECM) proteins osteopontin and fibronectin and the basement membrane proteins collagen IV and laminin I. TRAP-induced properties were reverted upon shRNA-mediated knockdown of TRAP or treatment with the small molecule TRAP inhibitor 5-PNA. Global phosphoproteomics and proteomics analyses identified possible substrates of TRAP phosphatase activity or signaling intermediates and outlined a TRAP-dependent regulation of proteins involved in cell adhesion and ECM organization. Upregulation of TGFβ isoform 2 (TGFβ2), TGFβ receptor type 1 (TβR1) and Mothers against decapentaplegic homolog 2 (SMAD2), as well as increased intracellular phosphorylation of CD44 were identified upon TRAP perturbation. Functional antibody-mediated blocking and chemical inhibition demonstrated that TRAP-dependent migration and proliferation is regulated via TGFβ2/TβR, whereas proliferation beyond basal levels is regulated through CD44.
conclusionAltogether, TRAP promotes metastasis-related cell properties in MDA-MB-231 breast cancer cells via TGFβ2/TβR and CD44, thereby identifying a potential signaling mechanism associated to TRAP action in breast cancer cells.
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